6533b7d9fe1ef96bd126b961
RESEARCH PRODUCT
Insufficient generation of Th17 cells in IL-23p19-deficient BALB/c mice protects against progressive cutaneous leishmaniasis
Beate LorenzEsther Von StebutBeatrix SchumakSusanna Lopez KostkaAndré GessnerKirsten Dietze-schwonbergsubject
0301 basic medicinemedicine.medical_treatmentLeishmaniasis CutaneousDermatologyPolymerase Chain ReactionBiochemistryBALB/cInterferon-gammaMice03 medical and health sciences0302 clinical medicineImmune systemCutaneous leishmaniasisInterferonInterleukin 23AnimalsMedicineMolecular BiologyLeishmania majorMice Inbred BALB Cbiologybusiness.industryLeishmaniasisDendritic CellsLeishmaniabiology.organism_classificationmedicine.disease030104 developmental biologyCytokineImmunologyDisease ProgressionInterleukin-23 Subunit p19CytokinesTh17 Cellsbusiness030215 immunologymedicine.drugdescription
Healing of leishmaniasis-a parasitic skin disease-is associated with high levels of secreted interferon (IFN)γ and IL-12 in resistant C57BL/6 mice and humans. Susceptible BALB/c mice predominantly react with a Th17/Th2/Treg-related immune response and finally succumb to infection. Previously, we showed that BALB/c IL-17A-/- mice are protected against Leishmania (L.) major infections, indicating that IL-17A-predominantly produced by Th17 cells-plays an important role for disease outcome. We now investigated DC-derived cytokines and finally identified IL-23p19 as key cytokine responsible for induction of Leishmania-specific Th17 cells that play an important role for progressive disease in susceptible BALB/c mice.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2017-12-06 | Experimental Dermatology |